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CD93通过通过p38MAPK/MK2/HSP27轴促进血管生成来改善糖尿病伤口

Yuan Xu¹, Yuhuan Jia¹, Na Wu¹

¹College of Stomatology, Chongqing Medical University, Chongqing, China; Chongqing Key Laboratory of Oral Diseases and Biomedical Sciences, Chongqing, China; Chongqing Municipal Key Laboratory of Oral Biomedical Engineering of Higher Education, Chongqing, China.

European journal of vascular and endovascular surgery : the official journal of the European Society for Vascular Surgery

|June 9, 2023

概括

CD93蛋白质促进新的血管形成 (血管生成) 并改善糖尿病伤口的愈合. 这种分子激活了一个关键的信号通路,为糖尿病伤口修复提供了潜在的治疗点.

科学领域:

血管生物学血管生物学
伤口治愈研究研究伤口治愈研究
糖尿病并发症糖尿病并发症

背景情况:

糖尿病伤口是由于血液供应和代谢交换不良而引起的,因此需要加强局部血管生成的治疗来治愈.
在之前的研究中,CD93在内皮细胞上表达,已显示出作为血管生成分子的潜力.
在糖尿病伤口愈合的背景下,CD93的特定作用仍未得到研究.

研究的目的:

研究CD93在促进糖尿病患者血管生成和伤口愈合中的作用和机制.
评估CD93在加速糖尿病伤口修复中的治疗潜力.

主要方法:

评估了CD93对血管生成的外源和内源影响 in vitro (使用微血管内皮细胞) 和 in vivo (在小鼠中).
利用CD93淘汰和野生型糖尿病小鼠分析伤口愈合,新血管化和重新上皮化.
通过检查CD93对内皮细胞中p38MAPK/MK2/HSP27信号通路的影响来研究分子机制.

主要成果:

外源的CD93蛋白促进了内皮细胞管的形成,发芽和血管结构的发展,加速了伤口愈合.
CD93缺陷损害了伤口修复,显示了降低的新血管化,血管成熟和重新表皮化.
确定p38MAPK/MK2/HSP27通路的CD93激活是其亲血管性功能的关键机制.

结论:

在体外和体内,CD93显著促进血管生成,通过p38MAPK/MK2/HSP27通路进行介导.
CD93通过增强血管生成和再上皮化,对糖尿病伤口愈合产生有益影响.

关键词:

血管新生的产生.CD93 CD93 CD93 CD93 CD93 CD93 CD93 CD93 CD93 CD93 CD93 CD93 糖尿病的伤口重新上皮化 (re-epithelisation) 的情况.p38MAPKKK 在线阅读

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